RESUMO
Equine influenza is a highly contagious disease caused by the H3N8 equine influenza virus (EIV), which is endemically distributed throughout the world. It infects equids, and interspecies transmission to dogs has been reported. The H3N8 Florida lineage, which is divided into clades 1 and 2, is the most representative lineage in the Americas. The EIV infects the respiratory system, affecting the ciliated epithelial cells and preventing the elimination of foreign bodies and substances. Certain factors related to the disease, such as an outdated vaccination plan, age, training, and close contact with other animals, favor the presentation of equine influenza. This review focuses on the molecular, pathophysiological, and epidemiological characteristics of EIV in the Americas to present updated information to achieve prevention and control of the virus. We also discuss the need for monitoring the disease, the use of vaccines, and the appropriate application of those biologicals, among other biosecurity measures that are important for the control of the virus.
RESUMO
Background: Despite the fact that Helicobacter spp. has been detected in equine gastric mucosa, no evidence exists about this infection in Colombian horses affected by equine ulcerative gastric syndrome (EGUS), nor in dental tartar. Objective: To detect Helicobacter spp. DNA in equine gastric mucosa and dental tartar and determine the relationship between the presence of Helicobacter spp. and gastric lesions. Methods: Samples of glandular gastric mucosa and dental tartar were collected from 30 equine slaughterhouses. Macroscopic lesions of the stomachs were classified and the total DNA in all samples was extracted using a commercial extraction kit. A final-point PCR was performed using primers for amplification of a segment of 251 bp of the gene encoding the 16s rRNA region; the amplified fragments were subjected to a second PCR to determine the presence of H. pylori, the VacA gene was typified. The resulting amplicons were sequenced. Results: It was possible to amplify 16s rRNA in several samples but there was no amplification of VacA. Fragments of the sequences were compatible with H. heilmannii. The 23.3 and 10% of gastric and tartar samples were positive for 16s rRNA of Helicobacter spp., respectively. Conclusion: Although genetic material of Helicobacter spp. was found in some animals, there was no relationship with gastric lesions. It is possible that helicobacteriosis has no bearing in EGUS etiology.
Antecedentes: A pesar de que se ha detectado Helicobacter spp. en mucosa gástrica equina, no existe evidencia de esta infección en caballos criollos colombianos afectados por síndrome ulcerativo gástrico (SUGE), ni tampoco reportes en sarro dental. Objetivo: Detectar ADN de Helicobacter spp. en sarro dental y mucosa gástrica de equinos, y determinar la relación entre la presencia de la bacteria y lesiones gástricas. Métodos: Las muestras de mucosa glandular gástrica y sarro dental fueron colectadas de 30 equinos que se encontraban en planta de beneficio. Las lesiones macroscópicas fueron clasificadas y el ADN total de las muestras fue extraído utilizando un kit comercial. Se desarrolló PCR convencional usando cebadores específicos para la amplificación de un segmento de 251 pb de un gen que codifica la región 16S del ARNr; los fragmentos amplificados fueron sometidos a una segunda PCR para determinar la presencia de H. pylori mediante la amplificación del gen VacA. Los amplificados resultantes fueron secuenciados. Resultados: Fue posible amplificar 16s ARNr en varias muestras, pero no hubo amplificación de VacA. Los fragmentos de las secuencias fueron compatibles con H. heilmannii. El 23,3 y 10% de las muestras gástricas y sarro fueron positivas para 16s ARNr de Helicobacter spp., respectivamente. Conclusión: Aunque el material genético de Helicobacter spp. se encontró en algunos animales, no hubo relación con las lesiones gástricas. Es posible que la helicobacteriosis no tenga incidencia en la etiología del EGUS.
Antecedentes: Apesar do Helicobacter spp. ter sido detectado na mucosa gástrica de equinos, não há evidências dessa infecção em cavalos crioulos colombianos afetados pela síndrome ulcerativa gástrica (SUGE), ou no sarro. Objetivo: Detectar ADN de Helicobacter spp. na mucosa gástrica e do sarro dental de equinos, e determinar a relação entre a presença de Helicobacter spp. e lesões gástricas. Métodos: Amostras de mucosa gástrica glandular e sarro dental foram coletadas de 30 equinos de abatedouro, as lesões macroscópicas dos estômagos foram classificadas. Se realizou extração de ADN total em todas as amostras através de kit comercial. Realizou-se PCR ponto final, amplificando o segmento de 251 pb do gene que codifica para a região 16s ARNr; os fragmentos amplificados foram sometidos novamente a PCR para determinar a presença de H. pylori, ao tipificar o gene VacA, e seguidamente foram sequenciados. Resultados: O houve amplificação do 16s ARNr em várias amostras, mas não amplificação de VacA. Fragmentos das sequencias foram compatíveis com H. heilmannii. O 23,3 e 10% das amostras gástricas e do sarro foram positivas para 16s ARNr de Helicobacter, respectivamente. Conclusão: Embora material genético de Helicobacter spp. encontrou-se em algumos animais não houve relação com lesões gástricas. Possivelmente a helicobacterioses não tem papel relevante na etiologia da SUGE.